{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yabas M"],"funding":["NIAID NIH HHS","Wellcome Trust"],"pagination":["441-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3272780"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(5)"],"pubmed_abstract":["Subcompartments of the plasma membrane are believed to be critical for lymphocyte responses, but few genetic tools are available to test their function. Here we describe a previously unknown X-linked B cell-deficiency syndrome in mice caused by mutations in Atp11c, which encodes a member of the P4 ATPase family thought to serve as 'flippases' that concentrate aminophospholipids in the cytoplasmic leaflet of cell membranes. Defective ATP11C resulted in a lower rate of phosphatidylserine translocation in pro-B cells and much lower pre-B cell and B cell numbers despite expression of pre-rearranged immunoglobulin transgenes or enforced expression of the prosurvival protein Bcl-2 to prevent apoptosis and abolished pre-B cell population expansion in response to a transgene encoding interleukin 7"],"journal":["Nature immunology"],"pubmed_title":["ATP11C is critical for the internalization of phosphatidylserine and differentiation of B lymphocytes."],"pmcid":["PMC3272780"],"funding_grant_id":["U54 AI054523","U54 AI054523-01","U54 AI054523-04","U54 AI054523-02","U54 AI054523-03"],"pubmed_authors":["Whittle B","Goodnow CC","Farell GC","Sprent J","Tze LE","Lal D","Enders A","Roots CM","Andrews DT","Broer S","Kucharska EM","Frankenreiter S","Zhang Y","Yabas M","Kofler J","Teoh NC","Teh CE"],"additional_accession":[]},"is_claimable":false,"name":"ATP11C is critical for the internalization of phosphatidylserine and differentiation of B lymphocytes.","description":"Subcompartments of the plasma membrane are believed to be critical for lymphocyte responses, but few genetic tools are available to test their function. Here we describe a previously unknown X-linked B cell-deficiency syndrome in mice caused by mutations in Atp11c, which encodes a member of the P4 ATPase family thought to serve as 'flippases' that concentrate aminophospholipids in the cytoplasmic leaflet of cell membranes. Defective ATP11C resulted in a lower rate of phosphatidylserine translocation in pro-B cells and much lower pre-B cell and B cell numbers despite expression of pre-rearranged immunoglobulin transgenes or enforced expression of the prosurvival protein Bcl-2 to prevent apoptosis and abolished pre-B cell population expansion in response to a transgene encoding interleukin 7","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 May","modification":"2025-04-18T19:53:27.637Z","creation":"2019-03-27T00:48:46Z"},"accession":"S-EPMC3272780","cross_references":{"pubmed":["21423173"],"doi":["10.1038/ni.2011"]}}